Abstract
AIM: To explore the protective effects of melatonin (Mel) on the abnormal phosphorylation of neuronal cytoskeletal proteins. METHODS: We generated a neuroblastoma (SH-SY5Y) cell system in which cytoskeletal proteins are abnormally phosphorylated resulting in microtubule disruption due to the marked inhibition of protein phosphatase activities by okadaic acid (OA). RESULTS: OA-induced declines in cell viability and mitochondrial metabolic activity were remarkably prevented by Mel. In addition, the hyperphosphorylation/accumulation of neurofilament-(NF-) H/M subunits and the disruption of microtubules, induced by OA, were significantly inhibited by Mel. CONCLUSION: Our results suggest multiple protective functions of Mel against a series of pathological lesions known to culminate in AD, including abnormal phosphorylation of cytoskeletal proteins, microtubule disassembly and mitochondrion-initiated cell toxicity.
| Original language | English |
|---|---|
| Pages (from-to) | 276-280 |
| Number of pages | 5 |
| Journal | Acta Pharmacologica Sinica |
| Volume | 25 |
| Issue number | 3 |
| Publication status | Published - 1 Mar 2004 |
| Externally published | Yes |
Keywords
- Alzheimer disease
- Melatonin
- Neurofilament proteins
- Okadaic acid
- Protein phosphatase